National Institutes of Health researchers found that a single, low-dose ketamine infusion was relatively free of side effects for patients with treatment-resistant depression. Elia Acevedo-Diaz, M.D., Carlos Zarate, M.D., and colleagues at the NIH’s National Institute of Mental Health (NIMH) report their findings in the Journal of Affective Disorders. Studies have shown that a single, subanesthetic-dose (a lower dose than would cause anesthesia) ketamine infusion can often rapidly relieve depressive symptoms within hours in people who have not responded to conventional antidepressants, which typically take weeks or months to work. However, widespread off-label use of intravenous subanesthetic-dose ketamine for treatment-resistant depression has raised concerns about side effects, especially given its history as a drug of abuse. “The most common short-term side effect was feeling strange or loopy,” said Acevedo-Diaz, of the Section on the Neurobiology and Treatment of Mood Disorders, part of the NIMH Intramural Research Program (IRP) in Bethesda, Maryland. “Most side effects peaked within an hour of ketamine administration and were gone within two hours. We did not see any serious, drug-related adverse events or increased ketamine cravings with a single-administration.” The researchers compiled data on side effects from 163 patients with major depressive disorder or bipolar disorder and 25 healthy controls who participated in one of five placebo-controlled clinical trials conducted at the NIH Clinical Center over 13 years. While past studies have been based mostly on passive monitoring, the NIMH IRP assessment involved active and structured surveillance of emerging side effects in an inpatient setting and used both a standard rating scale and clinician interviews. In addition to dissociative (disconnected, unreal) symptoms, the NIMH IRP assessment examined other potential side effects — including headaches, dizziness, and sleepiness. The study did not address the side effects associated with repeated infusions or long-term use.

Keyword: Depression
Link ID: 26822 - Posted: 11.16.2019

Emily Makowski China’s approval of the drug oligomannate earlier this month for treating mild to moderate Alzheimer’s disease has been met with surprise and skepticism from some members of the scientific community, who claim that the preclinical data raise questions about the underlying mechanism of the drug. One microbiome researcher has pointed out inconsistencies between the researchers’ data and their proposed mechanism for how oligomannate could treat Alzheimer’s. “The field is seeing this [research] with a large dose of skepticism,” Malú Tansey, a neuroimmunologist at the University of Florida College of Medicine, tells The Scientist. On November 2, Shanghai Green Valley Pharmaceuticals announced that oligomannate, an oligosaccharide mixture derived from brown algae, had been approved by the National Medical Product Administration (NMPA), China’s equivalent of the US Food and Drug Administration. The announcement followed the completion of a Phase 3 clinical trial in China that found the drug appeared to slow cognitive decline in Alzheimer’s patients. In addition, researchers led by Meiyu Geng at the Shanghai Institute of Materia Medica published a paper in Cell Research in September on oligomannate’s ability to remodel the gut microbiome in mice and reduce neuroinflammation. There is an emerging link between the gut microbiome and Alzheimer’s disease in humans. In the study, the researchers gave oligomannate to mice that are genetically engineered to show physical and behavioral symptoms similar to Alzheimer’s disease. The team collected mouse feces to study the microorganisms present in gut microbiota, drew blood to analyze the presence of immune cells, and also examined the levels of cytokines, which are inflammatory compounds, in the brain. © 1986–2019 The Scientist

Keyword: Alzheimers
Link ID: 26821 - Posted: 11.16.2019

By David S. Ludwig and Steven B. Heymsfield Most diet trials in the best journals fail even the most basic of quality control measures. That’s the finding of a study by us to be published today in JAMA Network Open. Investigators receiving funding for any clinical trial from the National Institutes of Health must register in advance what they plan to test, among other design features, to ensure that the data are fairly analyzed. Comparing the original registries with the final published studies, we found that diet trials in the past decade were about four times as likely as drug trials to have a discrepancy in the main outcome or measurement — raising concern for bias. This quality-control problem of diet trials in comparison to ones on pharmaceuticals leads to a bigger issue: underinvestment in nutrition research and in how we tackle the mysteries of a healthy diet. Although the problems with observational studies have received much attention (“Association doesn’t prove causation,” as scientists say), clinical trials can suffer from equally important limitations. In a clinical trial, investigators assign volunteers to receive different treatments — such as a a low-carbohydrate versus low-fat diet — ideally in random order. Beyond registry issues, trials may provide misleading results for many reasons, including small size, short duration and weak interventions (they lack power to actually make the intended change in behavior). These failures are disturbing because epidemics of diet-related disease will shorten life expectancy and impose huge economic costs on the United States in coming years. We continue to lack effective dietary prevention, in part because clinical trials have been too poorly designed and conducted to reach definitive conclusions. We’re still debating questions that have raged for decades: Should we focus on reducing carbs or fat? Is red meat harmful? Is sugar toxic? What about artificially sweetened beverages or moderate amounts of alcohol? © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26820 - Posted: 11.14.2019

By Gary Stix Socrates famously railed against the evils of writing. The sage warned that it would “introduce forgetfulness into the soul of those who learn it: they will not practice using their memory because they will put their trust in writing.” He got a few things wrong. For one, people nurture Socrates’ memory because of all of the books written about him. But he also was off the mark in his musings about a forgetfulness of the soul. If anything, it appears that just the opposite holds: a study of hundreds of illiterate people living at the northern end of an island considered to be a world media capital roundly contradicts the father of Western philosophy. Evaluations of the elderly in the environs of Manhattan’s Washington Heights (the neighborhood immortalized by a Lin-Manuel Miranda musical) reveal that the very act of reading or writing—largely apart from any formal education—may help protect against the forgetfulness of dementia. “The people who were illiterate in the study developed dementia at an earlier age than people who were literate in the study,” says Jennifer J. Manly, senior author of the paper, which appeared on November 13in Neurology. Earlier studies trying to parse this topic had not been able to disentangle the role of reading and writing from schooling to determine whether literacy, by itself, could be a pivotal factor safeguarding people against dementia later in life. The researchers conducting the new study, who are mostly at Columbia University’s Vagelos College of Physicians and Surgeons, recruited 983 people with four years or less of schooling who were part of the renowned Washington Heights–Inwood Columbia Community Aging Project. Of that group, 238 were illiterate, which was determined by asking the participants point-blank, “Did you ever learn to read or write?”—followed by reading tests administered to a subsample. Even without much time in school, study subjects sometimes learned from other family members. © 2019 Scientific American

Keyword: Alzheimers; Language
Link ID: 26819 - Posted: 11.14.2019

By Bruce Bower An ancient ape that was larger than a full-grown male gorilla has now revealed molecular clues to its evolutionary roots. Proteins extracted from a roughly 1.9-million-year-old tooth of the aptly named Gigantopithecus blacki peg it as a close relative of modern orangutans and their direct ancestors, say bioarchaeologist Frido Welker of the University of Copenhagen and his colleagues. Protein comparisons among living and fossil apes suggest that Gigantopithecus and orangutan forerunners diverged from a common ancestor between around 10 million and 12 million years ago, Welker’s group reports November 13 in Nature. Since it was first described in 1935, based on a molar purchased from a traditional Chinese drugstore in Hong Kong, G. blacki has stimulated debate over its evolutionary links to other ancient apes. Almost 2,000 isolated teeth and four partial jaws of G. blacki have since been found in southern China and nearby parts of Southeast Asia. G. blacki fossils date from around 2 million to almost 300,000 years ago. The sizes of individual teeth and jaws indicate that G. blacki weighed between 200 and 300 kilograms. Proteins preserve better in teeth and bones than DNA does, but both molecular forms break down quickly in hot, humid settings. “We were surprised to find any proteins this old at all, especially in a fossil from a subtropical environment,” Welker says. Proteins consisting of chains of amino acids can be used to sort out living and fossil species of various animals, including hominids (SN: 5/1/19). © Society for Science & the Public 2000–2019

Keyword: Evolution
Link ID: 26818 - Posted: 11.14.2019

By Karinna Hurley Part of the Museum of Natural History in Paris, the Jardin des Plantes, on the left bank of the Seine River, hosts a collection of galleries and gardens. A couple of miles away, the larger museum also includes the Museum of Mankind, which is, in part, an exploration of what it means to be human. There, like in many other museums worldwide, you can view a collection of stone tools used by the earliest humans. Tool use was long believed to be unique to our species—a defining feature, like language. Utilizing objects to achieve goals is not just a demonstration of advanced cognitive capabilities; it is largely through our symbolic and material tools that we share and transmit culture. In 1960 primatologist Jane Goodall observed wild chimpanzees making and using tools. A connection between humans and other animals, in how we think and learn, was captivating news. Since then, scientists have gone on to establish tool use in a relatively small number of other species. And observations of learning to use a tool from other group members, rather than instinctively, have been even more rare—until now. The Jardin des Plantes is also home to a special couple, Priscilla and Billie. Along with at least one of their daughters, these Visayan warty pigs—residents of the garden’s zoo—are the first in any pig species to be identified using tools and, even more remarkably, to apparently transmit this behavior through social learning. The discovery was made by chance by ecologist Meredith Root-Bernstein, who was watching the family from outside its enclosure. Priscilla, working on building a nest, picked up a piece of bark in her mouth and used it to aid her digging. For six weeks Root-Bernstein frequently returned to the zoo to try to again catch her in the act. Although she didn’t do so, she did notice the digging tool moved among different areas of the enclosure and always near a recently constructed nest. © 2019 Scientific American

Keyword: Evolution; Intelligence
Link ID: 26817 - Posted: 11.14.2019

Catherine Offord A clinical trial of a gene therapy for Duchenne muscular dystrophy has been halted after a patient suffered serious side effects following treatment, Reuters reports today (November 12). After receiving Solid Biosciences’s experimental therapy, SGT-001, the patient experienced kidney injury and drops in red blood cell count, leading the US Food and Drug Administration (FDA) to place the study on hold. “We are encouraged that this patient is recovering,” Ilan Ganot, Solid Biosciences’s CEO, president, and cofounder, says in a statement. “In the coming weeks, we anticipate that we will have a better understanding of the biological activity and potential benefit of SGT-001. We look forward to sharing this additional data and working with the FDA to resolve the clinical hold and determining next steps for the program.” SGT-001 has been administered to six people so far, and involves the transfer of an engineered version of the dystrophin gene DMD, which is dysfunctional in people with Duchenne muscular dystrophy, using an adeno-associated virus (AAV) as a vector. Sarepta Therapeutics, Pfizer, and other biopharmaceutical companies are investigating similar approaches to treat the condition, although the choice of AAV varies. See “Positive Trial Results for Experimental DMD Gene Therapy” This isn’t the first time Solid Biosciences’s trial of SGT-001 has been put on hold. Early last year, the FDA halted the same study after a patient receiving a low dose of the therapy experienced a drop in red blood cell count and had to be hospitalized. The company was allowed to resume the trial last June after making changes to the study design. © 1986–2019 The Scientist

Keyword: Movement Disorders; Muscles
Link ID: 26816 - Posted: 11.14.2019

By Kristopher Nielsen Have you ever heard of a condition known as “general paresis of the insane”? Probably not. In the 19th century general paresis was one of the most commonly diagnosed mental disorders. Its symptoms included odd social behaviors, impaired judgment, depressed mood and difficulty concentrating. Around the turn of the 20th century, though, we figured what it really was—a form of late-stage syphilis infecting the brain and disrupting its function. A few decades later we discovered a highly effective treatment: penicillin. Although general paresis is now very rare, its example is still instructive. Any honest researcher will tell you we don’t currently have good explanations for most mental disorders. Depression, obsessive-compulsive disorder, schizophrenia—we don’t really know how these patterns of disrupted thought, behavior and emotion develop or why they stick around. Yet the hope remains that, much like with general paresis, we may soon discover the root causes of these illnesses, and this knowledge may tell us how to treat them. An example of this hope can be seen in the popular notion that a “chemical imbalance” causes depression. This might turn out to be true, but the truth is we don’t know. Some researchers are starting to think that for many mental disorders, such hope might be based on incorrect assumptions. Instead of having one root cause, as general paresis did, mental disorders might be caused by many mechanisms acting together. These mechanisms might be situated in the brain, but they could also be located in the body and even in the external environment, interacting with one another in a network to create the patterns of distress and dysfunction we currently recognize and label as varieties of mental illness. In this more complex view, patterns such as depression and generalized anxiety arise as tendencies in the human brain-body-environment system. Once the patterns are established, they are hard to change because the network continues to maintain them. © 2019 Scientific American

Keyword: Schizophrenia; Depression
Link ID: 26815 - Posted: 11.12.2019

Hate eating certain vegetables? It could be down to your genes, say US scientists who have done some new research. Inheriting two copies of the unpleasant taste gene provides a "ruin-your-day level of bitterness" to foods like broccoli and sprouts, they say. It could explain why some people find it difficult to include enough vegetables in their diet, they suggest. The gene may also make beer, coffee and dark chocolate taste unpleasant. In evolutionary terms, being sensitive to bitter taste may be beneficial - protecting humans from eating things that could be poisonous. But Dr Jennifer Smith and colleagues from the University of Kentucky School of Medicine say it can also mean some people struggle to eat their recommended five-a-day of fresh fruit and veg. Everyone inherits two copies of a taste gene called TAS2R38. It encodes for a protein in the taste receptors on the tongue which allows us to taste bitterness. People who inherit two copies of a variant of the gene TAS2R38, called AVI, are not sensitive to bitter tastes from certain chemicals. Those with one copy of AVI and another called PAV perceive bitter tastes of these chemicals, but not to such an extreme degree as individuals with two copies of PAV, often called "super-tasters", who find the same foods exceptionally bitter. The scientists studied 175 people and found those with two copies of the bitter taste PAV version of the gene ate only small amounts of leafy green vegetables, which are good for the heart. Dr Smith told medics at a meeting of the American Heart Association: "You have to consider how things taste if you really want your patient to follow nutrition guidelines." © 2019 BBC.

Keyword: Chemical Senses (Smell & Taste); Genes & Behavior
Link ID: 26814 - Posted: 11.12.2019

By Nicholas Bakalar Poor sleepers may be at increased risk for cardiovascular disease. Chinese researchers used data on 487,200 people ages 30 to 79, generally healthy at the start of the study. The participants reported on the frequency of three symptoms of poor sleep: difficulty falling or staying asleep, daytime sleepiness and early morning awakening. The study is in Neurology. The scientists followed the group for an average of 10 years, during which there were 130,032 cases of cardiovascular disease. After adjusting for age, alcohol consumption, family history of cardiovascular disease and many other factors, they found that difficulty falling asleep was associated with a 9 percent increased relative risk for cardiovascular disease, early morning awakening with a 7 percent increased risk, and daytime sleepiness with a 13 percent increased risk. Compared with those who had no sleep problems, those with all three symptoms had an 18 percent increased relative risk of cardiovascular disease. The link was especially strong in younger people. The lead author, Canqing Yu, an associate professor at Peking University, noted that the sleep data depended on self-reports, and this observational study does not prove cause and effect. “People with difficulty sleeping shouldn’t be alarmed by this finding,” he said. “Poor sleep is a minor contributor to cardiovascular disease. But among young people who have no other risk factors, this can be important.” © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26813 - Posted: 11.12.2019

By Veronique Greenwood When a bird preens its feathers, it uses a little of nature’s own pomade: an oil made by glands just above the tail. This oil helps clean and protect the bird’s plumage, but also contains a delicate bouquet of scents. To other birds — potential mates or would-be rivals — these smells carry many messages, not unlike the birdsongs and fancy feathers that are more obvious to human observers. These scents may signal that a bird would be dangerous to encounter or might be ready to mate, or any number of other cues. However, new research using dark-eyed juncos, a common North American bird, suggests that these odoriferous messages may not be entirely of the bird’s own making. In a study published last month in the Journal of Experimental Biology, biologists reported that microbes living peacefully on the birds’ oil glands may play an important role in making the scent molecules involved. That implies that the birds’ microbiomes may influence both the smell and the behavior it provokes in other birds. Birds’ scented messages are the focus of the research of Danielle Whittaker, managing director of the Beacon Center for the Study of Evolution in Action at Michigan State University and an author of the paper. Some years ago, after she gave a talk, Kevin Theis, a colleague who studied scent-producing bacteria living on hyenas and who is a co-author of the new paper, asked her whether she had ever looked at the birds’ microbes. “I had never thought about bacteria at all,” said Dr. Whittaker. “But all the compounds I was describing were known byproducts of bacterial metabolism.” Dr. Whittaker took samples of bacteria living on the oil glands of 10 captive dark-eyed juncos and then injected the glands with an antibiotic. When she compared the microbes before and after the treatment, the results seemed to show that two groups of bacteria in particular had taken a hit from the treatment. Furthermore, when she compared the scent molecules in the oil before and after the treatment, there were significant differences. © 2019 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 26812 - Posted: 11.11.2019

By Gabriel Finkelstein Unlike Charles Darwin and Claude Bernard, who endure as heroes in England and France, Emil du Bois-Reymond is generally forgotten in Germany — no streets bear his name, no stamps portray his image, no celebrations are held in his honor, and no collections of his essays remain in print. Most Germans have never heard of him, and if they have, they generally assume that he was Swiss. But it wasn’t always this way. Du Bois-Reymond was once lauded as “the foremost naturalist of Europe,” “the last of the encyclopedists,” and “one of the greatest scientists Germany ever produced.” Contemporaries celebrated him for his research in neuroscience and his addresses on science and culture; in fact, the poet Jules Laforgue reported seeing his picture hanging for sale in German shop windows alongside those of the Prussian royal family. Those familiar with du Bois-Reymond generally recall his advocacy of understanding biology in terms of chemistry and physics, but during his lifetime he earned recognition for a host of other achievements. He pioneered the use of instruments in neuroscience, discovered the electrical transmission of nerve signals, linked structure to function in neural tissue, and posited the improvement of neural connections with use. He served as a professor, as dean, and as rector at the University of Berlin, directed the first institute of physiology in Prussia, was secretary of the Prussian Academy of Sciences, established the first society of physics in Germany, helped found the Berlin Society of Anthropology, oversaw the Berlin Physiological Society, edited the leading German journal of physiology, supervised dozens of researchers, and trained an army of physicians. © 2019 Scientific American

Keyword: Consciousness
Link ID: 26811 - Posted: 11.11.2019

Nicole Ireland · Recent video from Thailand showing paralyzed Humboldt Broncos hockey player Ryan Straschnitzki moving his legs after an electrical stimulation device was surgically implanted in his spine has sparked excitement — as well as questions — about therapies available to Canadians with spinal injuries. The procedure Straschnitzki, 20, had is called epidural stimulation, and although promising, it's still highly experimental, experts in both Canada and the U.S. say. It's in early stages of clinical trials in the U.S. and Europe to evaluate the safety and effectiveness of restoring physical abilities — from bowel and bladder function to moving arms and legs — to people who desperately want to get some normalcy back after spinal injury. Barry Munro understands all too well why people's immediate reaction is to ask why they can't try the procedure here in Canada. He's been hoping for — and working toward — finding a cure for spinal cord injury ever since he dove into a lake in his 20s and was left quadriplegic. Now 55, Munro is chief development officer for the Canadian Spinal Research Organization and works with the North American Spinal Injury Consortium. For more than 30 years, he's seen the headlines come and go, inciting hope that a cure is on the horizon. "I've been down this road before," Munro told CBC News. "I really, really believe in finding a cure and believe it will happen and I have that hope. But — there's a big but — we have to be careful." Milos Popovich, director of the KITE Research Institute at the University Health Network's Toronto Rehabilitation Institute, echoes that need to proceed with caution. He said that epidural stimulation must proceed through many more stages of scientifically sound clinical trials to prove it works before it could be made available as a therapy in Canada. ©2019 CBC/Radio-Canada.

Keyword: Regeneration; Movement Disorders
Link ID: 26810 - Posted: 11.11.2019

By Richard C. Paddock CIDAHU, Indonesia — Thousands of children with crippling birth defects. Half a million people poisoned. A toxic chemical found in the food supply. Accusations of a government cover-up and police officers on the take. This is the legacy of Indonesia’s mercury trade, a business intertwined with the lucrative and illegal production of gold. More than a hundred nations have joined a global campaign to reduce the international trade in mercury, an element so toxic there is “no known safe level of exposure,” according to health experts. But that effort has backfired in Indonesia, where illicit backyard manufacturers have sprung up to supply wildcat miners and replace mercury that was previously imported from abroad. Now, Indonesia produces so much black-market mercury that it has become a major global supplier, surreptitiously shipping thousands of tons to other parts of the world. Much of the mercury is destined for use in gold mining in Africa and Asia, passing through hubs such as Dubai and Singapore, according to court records — and the trade has deadly consequences. “It is a public health crisis,” said Yuyun Ismawati, a co-founder of an Indonesian environmental group, Nexus3 Foundation, and a recipient of the 2009 Goldman Environmental Prize. She has called for a worldwide ban on using mercury in gold mining. Mercury can be highly dangerous as it accumulates up the food chain, causing a wide range of disorders, including birth defects, neurological problems and even death. ImageA small mine on Sumbawa. Miners often dig for ore on land without permission or government permits. Today, despite the risks, small-scale miners using mercury operate in about 80 countries in Asia, Africa and the Americas. They produce up to 25 percent of all gold sold. © 2019 The New York Times Company

Keyword: Development of the Brain; Neurotoxins
Link ID: 26809 - Posted: 11.11.2019

By Denise Grady A form of vitamin E has been identified as a “very strong culprit” in lung injuries related to vaping THC, health officials reported on Friday, a major advance in a frightening outbreak that has killed 40 people and sickened 2,051. Many patients with the mysterious illness have wound up hospitalized in intensive care units, needing ventilators or even more desperate measures to help them breathe. Most are young, male adults or even teenagers. “For the first time, we have detected a potential toxin of concern, vitamin E acetate, from biological samples from patients,” with lung damage linked to vaping, Dr. Anne Schuchat, principal deputy director of the Centers for Disease Control and Prevention, said at a news briefing. The new report, based on samples taken from the lungs of 29 patients, including two who died, she said, “provided evidence of vitamin E acetate at the primary site of injury in the lungs.” She added, “These findings tell us what entered the lungs of some patients with these injuries.” The patients came from 10 states scattered around the country, so the findings are considered broadly applicable and unlikely to have resulted from a single vaping product or supplier. The results mesh with other research that found the vitamin compound in vaping products. But Dr. Schuchat left open the possibility that other chemicals or toxins from vaping fluids or devices could also be causing the severe respiratory ailments. The outbreak has revealed the existence of a vast, unregulated, shadowy marketplace of illicit or bootleg vaping products that are essentially a stew of unknown chemicals concocted, packed and sold by unknown manufacturers and sellers. © 2019 The New York Times Company

Keyword: Drug Abuse; Neurotoxins
Link ID: 26808 - Posted: 11.09.2019

Adam Miller · CBC News · New research is shedding light on how the brain interacts with music. It also highlights how challenging it is to study the issue effectively due to the highly personalized nature of how we interpret it. "Music is very subjective," says Dr. Daniel Levitin, a professor of neuroscience and music at McGill University in Montreal and author of the bestselling book This is Your Brain on Music. "People have their own preferences and their own experience and to some extent baggage that they bring to all of this — it is challenging." Levitin says there are more researchers studying the neurological effects of music now than ever before. From 1998 to 2008 there were only four media reports of evidence-based uses of music in research, while from 2009 to 2019 there were 185, Levitin said in a recent paper for the journal Music and Medicine. It's a "great time for music and brain research" because more people are well-trained and skilled at conducting rigorous experiments, according to Levitin. Emerging research reveals challenges A new study by researchers in Germany and Norway used artificial intelligence to analyze levels of "uncertainty" and "surprise" in 80,000 chords from 745 commercially successful pop songs on the U.S. Billboard charts. The research, published Thursday in Current Biology, found that chords provided more pleasure to the listener both when there is uncertainty in anticipating what comes next, and from the surprise the music elicits when the chords deviate from expectations. ©2019 CBC/Radio-Canada

Keyword: Hearing
Link ID: 26807 - Posted: 11.09.2019

New preclinical research reported in animal models shows that exposure to compounds found in marijuana called cannabinoids (CBs), which includes cannabidiol (CBD) and tetrahydrocannabinol (THC), during early pregnancy can cause malformations in the developing embryo. The research also demonstrated that co-exposure to CBs and alcohol increased the likelihood of birth defects involving the face and brain. The study, funded by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health, was published in Scientific Reports. “Prenatal alcohol exposure is a leading preventable cause of birth defects and neurodevelopmental abnormalities in the United States,” said NIAAA Director, George F. Koob, Ph.D. “Since marijuana and alcohol are frequently used simultaneously, the combined effects of cannabinoids and alcohol are worrisome as well as the dangers of either substance alone.” The detrimental effects of prenatal alcohol exposure on human development are well known and include an array of lifelong physical, cognitive, and behavioral problems collectively called fetal alcohol spectrum disorders (FASD). Alcohol can disrupt fetal development at any stage during pregnancy, even the earliest stages before a woman knows she is pregnant. The effects of marijuana exposure during pregnancy and the combined effect of alcohol and marijuana are less known. In the study, scientists led by Scott Parnell, Ph.D., at the Bowles Center for Alcohol Studies at the University of North Carolina in Chapel Hill, administered a variety of CBs alone and in combination with alcohol in varying amounts to mice on day eight of pregnancy, which is similar to the third and fourth weeks of pregnancy in humans. The CBD amounts administered were within what is considered a therapeutic range for several medical conditions in humans. The THC concentration administered was similar to levels reached by a person smoking marijuana.

Keyword: Development of the Brain; Drug Abuse
Link ID: 26806 - Posted: 11.09.2019

By Jake Buehler Tetrodotoxin, the chemical weapon of choice for pufferfish, is such a potent neurotoxin that a single animal contains enough poison to paralyze and kill dozens of predators, and even adult humans who dare to eat their delicate flesh. But new research suggests the poison serves another purpose for the fish entirely: stress relief. Japanese, or tiger, puffers (Takifugu rubripes) don’t make their own tetrodotoxin (TTX), but instead accumulate it in their organs and skin from TTX-making bacteria in their diet. Those raised in captivity tend to have different diets and, thus, lose their toxicity. To find out how the toxin affects developing fish, researchers augmented the diets of young, captive puffers with a dosage of purified TTX for 1 month. Puffers with replenished toxin stores grew a median of 6% longer and 24% heavier than those raised on a nontoxic diet. They were also less aggressive, nipping at each other’s tail fins less frequently. Growth rate and aggression are influenced by stress, so researchers also looked at levels of two stress-linked hormones: cortisol in the blood and corticotropin-releasing hormone in the brain. The nontoxic fish had higher levels of both, with a median level of cortisol four times that of the toxic fish, the researchers report online in Toxicon. © 2019 American Association for the Advancement of Science.

Keyword: Stress
Link ID: 26805 - Posted: 11.09.2019

By Tina Hesman Saey A newly discovered type of mitochondrial self-destruction may make some brain cells vulnerable to ALS, also known as Lou Gehrig’s disease. In mice genetically engineered to develop some forms of a degenerative nerve disease similar to amyotrophic lateral sclerosis, energy-generating organelles called mitochondria appear to dismantle themselves without help from usual cell demolition crews. This type of power plant self-destruction was spotted in upper motor neurons, brain nerve cells that help initiate and control movements, but not in neighboring cells, researchers report November 7 in Frontiers in Cellular Neuroscience. Death of those upper motor neurons is a hallmark of ALS, and the self-destructing mitochondria may be an early step that sets those cells up to die later. Pembe Hande Özdinler, a cellular neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and her colleagues have dubbed the mitochondrial dissolution “mitoautophagy.” It is a distinct process from mitophagy, the usual way that cellular structures called autophagosomes and lysosomes remove damaged mitochondria from the cell, Özdinler says. Usually, clearing out old or damaged mitochondria is important for cells to stay healthy. When mitochondria sustain too much damage, they may trigger the programmed death of the entire cell, known as apoptosis (SN: 8/9/18). Özdinler’s team spotted what she describes as “awkward” mitochondria in electron microscope images of upper motor neurons from 15-day-old mice. These unweaned mice are equivalent to human teenagers, Özdinler says. ALS typically doesn’t strike until people are 40 to 70 years old. But by the time symptoms appear, motor neurons are already damaged, so Özdinler’s group looked at the young mice to capture the earliest signs of the disease. © Society for Science & the Public 2000–2019

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26804 - Posted: 11.08.2019

Jon Hamilton There's new evidence that girls start out with the same math abilities as boys. A study of 104 children from ages 3 to 10 found similar patterns of brain activity in boys and girls as they engaged in basic math tasks, researchers reported Friday in the journal Science of Learning. "They are indistinguishable," says Jessica Cantlon, an author of the study and professor of developmental neuroscience at Carnegie Mellon University. The finding challenges the idea that more boys than girls end up in STEM fields (science, technology, engineering, and mathematics) because they are inherently better at the sort of thinking those fields require. It also backs other studies that found similar math abilities in males and females early in life. "The results of this study are not too surprising because typically we don't see sex differences at the ages assessed in this study or for the types of math tasks they did, which were fairly simple," says David Geary, a psychologist and curator's distinguished professor at the University of Missouri who was not involved in the research. But there is evidence of sex differences in some exceptional older students, Geary says. For example, boys outnumber girls by about three to one when researchers identify adolescents who achieve "very, very high-end performance in mathematics," Geary says, adding that scientists are still trying to understand why that gap exists. © 2019 npr

Keyword: Sexual Behavior; Learning & Memory
Link ID: 26803 - Posted: 11.08.2019